AG-20B-0005-TRIAL 25 µg
AG-20B-0005-C100 100 µg
Description
FLIP is an apoptosis regulator protein which functions as a crucial link between cell survival and cell death pathways in mammalian cells and acts as an inhibitor of TNFRSF6 mediated apoptosis. A proteolytic fragment (p43) is likely retained in the death-inducing signaling complex (DISC) thereby blocking further recruitment and processing of caspase-8 at the complex. Full length and shorter isoforms have been shown either to induce apoptosis or to reduce TNFRSF-triggered apoptosis. FLIP lacks enzymatic (caspase) activity. FLIP is highly expressed in skeletal muscle, pancreas, heart, kidney, placenta and peripheral blood leukocytes.
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AG-20B-0005 anti-FLIP, mAb (Dave-2)
I-FLICE; CLARP; CASPER; Usurpin, CASH; FLAME-1
Monoclonal Antibody
Recombinant human FLIP (aa 1-480).
Immunoprecipitation
Western Blot
Note: Not recommended for immunohistochemistry.Human
MouseRecognizes an epitope (aa 1-200) present in both short (FLIPS) and long (FLIPL) splice variants of human and mouse FLIP.
本產品短期保存請置於 4°C，長期保存建議分裝後存於 -20°C，可穩定保存至少一年，避免反覆凍融。
- Fas engagement induces the maturation of dendritic cells (DCs), the release of interleukin (IL)-1beta, and the production of interferon gamma in the absence of IL-12 during DC-T cell cognate interaction: a new role for Fas ligand in inf: M. Rescigno, et al.; J. Exp. Med. 192, 1661 (2000)
- Protein kinase C regulates FADD recruitment and death-inducing signaling complex formation in Fas/CD95-induced apoptosis: M. Gomez-Angelats & J.A. Cidlowski; J. Biol. Chem. 276, 44944 (2001)
- NF-kB signals induce the expression of c-FLIP: O. Micheau, et al.; Mol. Cell. Biol. 21, 5299 (2001)
- Fas-associated death domain protein (FADD) and caspase-8 mediate up-regulation of c-Fos by Fas ligand and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) via a FLICE inhibitory protein (FLIP)-regulated pathway: D. Siegmund, et al.; J. Biol. Chem. 276, 32585 (2001)
- Fas aggregation does not correlate with Fas-mediated apoptosis: Y. Lee & E. Shacter; J. Immunol. 167, 82 (2001)
- The caspase 8 inhibitor c-FLIP(L) modulates T-cell receptor-induced proliferation but not activation-induced cell death of lymphocytes: S.M. Lens, et al.; Mol. Cell. Biol. 22, 5419 (2002)
- Mitogen-Activated Protein Kinase/Extracellular Signal-Regulated Kinase Signaling in Activated T Cells Abrogates TRAIL-Induced Apoptosis Upstream of the Mitochondrial Amplification Loop and Caspase-8: T.S. Soderstrom, et al.; J. Immunol. 169, 2851 (2002)
- Characterization of the human FLICE-inhibitory protein locus and comparison of the anti-apoptotic activity of four different flip isoforms: M. Djerbi, et al.; Scand. J. Immunol. 54, 180 (2002)
- c-FLIP efficiently rescues TRAF-2-/- cells from TNF-induced apoptosis: C. Guiet, et al.; Cell Death Differ. 9, 138 (2002)
- Expression of the long form of human FLIP by retroviral gene transfer of hemopoietic stem cells exacerbates experimental autoimmune encephalomyelitis: M. Djerbi, et al.; J. Immunol. 170, 2064 (2003)
- Chemotherapy enhances TNF-related apoptosis-inducing ligand DISC assembly in HT29 human colon cancer cells: S. Lacour, et al.; Oncogene 22, 1807 (2003)
- Bile acids stimulate cFLIP phosphorylation enhancing TRAIL-mediated apoptosis: H. Higuchi, et al.; J. Biol. Chem. 278, 454 (2003)
- The anti-apoptotic factor Bcl-2 can functionally substitute for the B cell survival but not for the marginal zone B cell differentiation activity of BAFF: A. Tardivel, et al.; Eur. J. Immunol. 34, 509 (2004)
- Targeting Bcl-x(L) in esophageal squamous cancer to sensitize to chemotherapy plus TRAIL-induced apoptosis while normal epithelial cells are protected by blockade of caspase 9: K. Kim, et al.; Cell Death Differ. 11, 583 (2004)
- Fas-associated protein with death domain (FADD)-independent recruitment of c-FLIPL to death receptor 5: T.G. Jin, et al.; J. Biol. Chem. 279, 55594 (2004)
- The E3 ubiquitin ligase itch couples JNK activation to TNFalpha-induced cell death by inducing c-FLIP(L) turnover: L. Chang, et al.; Cell 124, 601 (2006)
- A Protective Role for the Human SMG-1 Kinase against Tumor Necrosis Factor-α-induced Apoptosis: V. Oliveira, et al.; J. Biol. Chem. 283, 13174 (2008)
- Cellular FLIP inhibits myeloid cell activation by suppressing selective innate signaling: YJ. Wu, et al.; Reproduction 150, 367 (2015)
- Knockdown of RIPK1 markedly exacerbates murine immune-mediated liver injury through massive apoptosis of hepatocytes, independent of necroptosis and inhibition of NF-κB: J. Suda, et al., J. Immunol. 197, 3120 (2016)
- The caspase-8 inhibitor emricasan combines with the SMAC mimetic birinapant to induce necroptosis and treat acute myeloid leukemia: G. Brumatti, et al.; Sci. Transl. Med. 8, 339ra69 (2016)
- TRAIL receptor gene editing unveils TRAIL-R1 as a master player of apoptosis induced by TRAIL and ER stress: D. Florent, et al.; Oncotarget 8, 9974 (2017)
- The Mitochondrial Apoptotic Effectors BAX/BAK Activate Caspase-3 and -7 to Trigger NLRP3 Inflammasome and Caspase-8 Driven IL-1β Activation: J.E. Vince, et al.; Cell Rep. 25, 2339 (2018)
- Necroptotic signaling is primed in Mycobacterium tuberculosis-infected macrophages, but its pathophysiological consequence in disease is restricted: M.D. Stutz, et al.; Cell Death Differ. 25, 951 (2018)
- Type I interferon signaling mediates Mycobacterium tuberculosis-induced macrophage death: L. Zhang, et al.; J. Exp. Med. 218, e20200887 (2021)
- Fibroblast growth factor 18 stimulates the proliferation of hepatic stellate cells, thereby inducing liver fibrosis:Y. Tsuchiya, et al.; Nature Commun. 14, 6304 (2023)